2003 Fiscal Year Final Research Report Summary
Elucidation of vasoreactive diversity induced by bradykinin -studies of G-proteins function and bradykinin metabolism -
| Project/Area Number |
13660302
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Basic veterinary science/Basic zootechnical science
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| Research Institution | Kagoshima University |
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Principal Investigator |
MIYAMOTO Atsushi Kagoshima University, Faculty of Agriculture, Associate professor, 農学部, 助教授 (70219806)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIO Akira Kagoshima University, Faculty of Agriculture, Professor, 農学部, 教授 (90133181)
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| Project Period (FY) |
2001 – 2003
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| Keywords | Bradykinin / Basilar artery / Vasoreactivity / Tyrosine phosphorylation / cultured endothelial cell / NO production / Losartan / HOE140 |
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| Research Abstract |
(1)Nitric oxide (NO) is spontaneously released from cultured porcine basilar arterial endothelial cells under no stimulation conditions. Bradykinin (BK) enhanced the NO production in a concentration-dependent manner. The enhanced NO production was inhibited by treatments of a selective B_2 receptor antagonist, HOE140, or a NO synthase inhibitor, L-nitro-arginine.
(2)Angiotensin (Ang) II induced a contraction in isolated porcine basilar arterial ring. A selective B_2 antagonist, HOE140, inhibited the AngII-induced contraction, while an Ang converting enzyme (ACE) inhibitor, captopril, enhanced the Ang II-induced contraction.
(3)BK induces endothelium-dependent relaxation following by contraction in isolated porcine basilar arterial ring. In the presence of L-nitro-arginine (10^<-4> M), BK induced contraction but not relaxation. The BK-induced contraction was not inhibited by a selective AT_1 receptor antagonist, losartan.
These results suggest that there might be some interaction between bradykinin and Ang receptors. Further experiments appears to be needed in this point.
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